Network Dynamics Mediate Circadian Clock Plasticity

Abdelhalim Azzi, Jennifer A. Evans, Tanya Leise, Jihwan Myung, Toru Takumi, Alec J. Davidson, Steven A. Brown

Research output: Contribution to journalArticlepeer-review

50 Citations (Scopus)


A circadian clock governs most aspects of mammalian behavior. Although its properties are in part genetically determined, altered light-dark environment can change circadian period length through a mechanism requiring de novo DNA methylation. We show here that this mechanism is mediated not via cell-autonomous clock properties, but rather through altered networking within the suprachiasmatic nuclei (SCN), the circadian “master clock,” which is DNA methylated in region-specific manner. DNA methylation is necessary to temporally reorganize circadian phasing among SCN neurons, which in turn changes the period length of the network as a whole. Interruption of neural communication by inhibiting neuronal firing or by physical cutting suppresses both SCN reorganization and period changes. Mathematical modeling suggests, and experiments confirm, that this SCN reorganization depends upon GABAergic signaling. Our results therefore show that basic circadian clock properties are governed by dynamic interactions among SCN neurons, with neuroadaptations in network function driven by the environment.

Original languageEnglish
Pages (from-to)441-450
Number of pages10
Issue number2
Publication statusPublished - Jan 18 2017
Externally publishedYes


  • automation
  • autopatcher
  • in vivo
  • patch clamp
  • subcortical
  • thalamus
  • whole-cell

ASJC Scopus subject areas

  • Neuroscience(all)


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